正常人外周血淋巴细胞 IL—2受体免疫放射测定

采用~(125)I 标记小鼠抗人IL—2受体(P55)的抗Tac(CD_(25))单克隆抗体,成功地建立了人IL—2受体的免疫放射分析法,动态观察了人外周血淋巴细胞经PHA 刺激24、48和72h 后IL—2受体表达的时间曲线,通过Scatchard 作图分析表明~(125)I—抗Tac 单克隆抗体与PHA 活化的上述三个时间点的T 淋巴细胞的最大结合容量(B_(max))分别为43000位点/细胞、54000位点/细胞和61000位点/细胞。本研究为临床IL—2受体检测提供一种简便的免疫放射测定法。     

急性高容量性血液稀释对妇科肿瘤患者围术期T淋巴细胞亚群的影响

目的探讨急性高容量性血液稀释(AHH)对妇科肿瘤患者围手术期T淋巴细胞亚群的影响.方法40例ASAⅠ～Ⅱ级的妇科肿瘤手术病人随机分成两组:高容量性血液稀释组(A组)在切皮前30分钟内输入6%羟乙基淀粉液1000ml;对照组(C组)常规输液,不实施血液稀释.分别与麻醉诱导前、手术结束后、术后24小时抽取静脉血,用流式细胞仪测定T淋巴细胞亚群CD3 、CD4 、CD8 及CD4 /CD8 细胞百分率.结果两组病人手术结束后(T1)、手术后第1天(T2)与麻醉诱导前(T0)比较:T淋巴细胞亚群CD3 、CD4 及CD4 CD8 均明显降低(P＜0.01或P＜0.05),CD8 无显著性变化;但A组手术结束后和手术后第1天CD3 、CD4 及CD4 /CD8 明显高于C组(P＜0.05).结论术前采用急性高容量性血液稀释(AHH),可显著改善妇科肿瘤患者T淋巴细胞的免疫功能.     

Effect of Inflammation on Costimulation Blockade-Resistant Allograft Rejection

Previously, we reported that allogeneic skin grafts were rapidly rejected by CD28 and CD40 ligand double deficient mice mediated by CD8⁺ T cells. These results indicated that some elements in addition to CD28- and CD40-mediated costimulation provide stimulatory signals for the activation of donor-specific CD8⁺ T cells. In this report, we investigated the role of inflammation associated with transplantation on costimulation-independent priming of CD8⁺ T cell during graft rejection. B6 RAG1 KO mice were transplanted with BALB/c-skin and adoptively transferred with syngeneic CD8⁺ T cells the same day or 50 days after transplantation. When blockade of CD28- and CD40-mediated costimulation failed to prevent acute rejection of freshly transplanted skin grafts, it efficiently delayed rejection of well-healed skin grafts. These results showed that factors associated with transplantation have essential roles in inducing costimulation blockade-resistant allograft rejection. Costimulation blockade failed to prevent acute graft-infiltration of NK cells and increasing expression of intragraft IL-12 and IL-15. These factors may trigger the graft-infiltration and priming of CD8⁺ T cells to induce costimulation blockade-resistant allograft rejection.     

Surface activation markers of T lymphocytes: role in the detection of infection in neonates

Diagnosis of perinatal infection in the newborn is difficult; there may be few clinical signs and current tests are slow or non-specific. Detection of organisms, antigen or specific antibody to common pathogens often requires repeat samples and does not give immediate results. Haematological parameters, although relied upon frequently to diagnose infection in the neonate prior to a positive bacterial isolation, are unreliable and insensitive. Indicators such as an increase in neutrophil band cell counts are highly variable between morphologists. Infection induces the expression of a number of T lymphocyte surface markers, including CD45RA/CD45RO and CD45RO. The use of changed expression of surface markers as a laboratory test for detection of infection in neonates was evaluated. We used multiparameter flow cytometry to detect expression of early (CD45RA/CD45RO) and late (CD45RO) activation markers. In the respective groups of 50 full term (including 25 normal vaginal deliveries and 25 caesarean deliveries) and 30 premature, i.e. < 36 weeks gestation (born by either normal vaginal delivery or caesarean delivery) the CD45RA isoform was brightly expressed on newborn ‘naive’ CD4⁺ T cells, whereas the CD45RO isoform (including both ‘bright’ and ‘dim’ populations) was present on < 19% of CD4⁺ T cells from these newborn infants. In a group of 37 infants, tested to evaluate possible effects of non-infective parameters such as respiratory distress and iso-immunization, no significant changes in surface marker expression were found and specificity of the test was confirmed. In 14 neonates with documented sepsis, up-regulation of dual staining CD45RA/CD45RO isoforms on CD4⁺ T cells was detected early in the infection. In addition, we found that CD45RO expression persisted for several weeks after bacterial infection, and up to several months in viral infection. In conclusion, detection of T cell activation by flow cytometry for the early diagnosis of neonatal infection is an easy test to carry out on small volumes of blood, is inexpensive, and may be a specific indicator of infection.     

Mammaplasty: Shape,volume, and scar size

Recently many mammaplasty techniques have been presented with special attention paid to the resulting scar's size and its position. The surgeon should try to hid the scar, and if the inverted T incision is used, its horizontal branch should be as short as possible and kept in the breast area. Neverthelss, excessive concern about the final scar size should not interfere with the final results of the mammaplasty as far as shape, volume and lasting results are concerned. The author presents his experience in mammaplasty with respect to the volume, the shape, and the scar size interrelationships.     

神经肽Y对免疫细胞活性的影响

神经肽Y（NPY）是广泛分布于中枢神经系统和外周神经各部位的神经肽类物质。本实验观察NPY在体外对几种免疫细胞活性的直接作用。结果表明，NPY对小鼠T淋巴细胞丝裂原反应性和NK细胞的杀伤活性均无明显影响（P＞0．05），对巨噬细胞分泌溶菌酶有明显抑制作用（P＜0．05）；而对B淋巴细胞丝裂原反应性则有明显的促进作用（P＜0．05）。上述结果提示，NPY对部分免疫细胞功能的影响因细胞种类而异。     

肺癌患者红细胞免疫功能和T淋巴细胞亚群的检测及临床意义

作者对62例肺癌患者进行红细胞免疫功能及T淋巴细胞亚群测定，并与20例正常人对照。结果显示：肺癌组红细胞膜C3b受体活性（RBC－C3bRR）、CD3 、CD4 、CD4 ／CD8 比值均低于正常人（P＜0．05～0．01），红细胞膜的吸附免疫复合物（RBC－ICR）、CD8 均高于正常人（P＜0．05～0．01），因此认为红细胞免疫及T淋巴细胞亚群测定对肺癌的诊断、治疗及病情预后估计有一定价值。     

脐血LAK细胞生物学特性影响因素的研究

采集２３名产妇的脐带血和８名正常成人的外周血制备ＬＡＫ细胞，随机分为４组，在培养第３，５，７，１４天，分别利用ＭＴＴ法和＾１２５Ｉ－ＵｄＲ释放法对４组ＬＡＫ细胞的增殖力和杀伤活性进行了测定，同时用细胞毒方法测定培养７天的ＬＡＫ细胞的免疫表型。结果发现，在不同培养时间，脐血来源的ＬＡＫ细胞增殖力显著高于成人血ＬＡＫ细胞（Ｐ〈０．０５或Ｐ〈０．０１），成人血清组，脐血血清组，红细胞组ＬＡＫ细胞增殖力有     

Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Actions on αT3-1 Gonadotrophs Show Desensitization

PACAP is a hypothalamic hypophysiotropic factor that acts upon a number of pituitary cells, including gonadotrophs. In the gonadotroph-derived αT3-1 cell line, PACAP acts via PVR1 receptors to stimulate adenylyl cyclase and phosphoinositidase C. PACAP-stimulated cAMP accumulation is inhibited by protein kinase C-activating phorbol esters in these cells and the current work was undertaken primarily to establish whether it is also subject to homologous regulation. In acute experiments, PACAP27-stimulated cAMP accumulation (intracellular plus extracellular) was measured (in the presence of phosphodiesterase inhibitor) both in intact cells and in cell membranes. The peptide increased cAMP accumulation, but initial rates of PACAP27-stimulated cAMP accumulation were reduced to between 10 and 50% within 10 min of stimulation in both cells and membranes. The initial rate of forskolin-stimulated cAMP accumulation was maintained in membranes but not in intact cells (although the deviation from linearity was less pronounced than with PACAP27). Thus, rapid homologous desensitization to PACAP27 occurs in intact αT3-1 cells, but is not entirely receptor specific. Rapid homologous desensitization of PACAP27-stimulated cAMP accumulation also occurred in the presence of a protein kinase C activating phorbol ester, which inhibited cAMP accumulation without altering the kinetics of the PACAP27 effect. Brief pre-treatment (3 min) with PACAP27 also reduced the ability of PACAP27, but not gonadotrophin-releasing hormone, to cause a spike-type elevation of cytosolic Ca²⁺ concentration (a consequence of phosphoinositidase C activation). In chronic desensitization studies, pre-treatment for 6 h with PACAP27 caused a dose-dependent (IC₅₀ approximately 10 nM) reduction of PACAP-stimulated cAMP accumulation and down regulated cell surface PVR1 receptors (to approximately 50%). Thus, it appears that PACAP27-stimulated (PVR-1 receptor mediated) adenylyl cyclase undergoes rapid homologous desensitization in αT3-1 cells, which is paralleled by homologous desensitization of PACAP27-stimulated phosphoinositidase C activity and involves mechanisms distinct from those underlying heterologous desensitization by phorbol esters. Chronic desensitization of PACAP-stimulated cAMP accumulation and down-regulation of cell surface PVR-1 receptors also occurs in these cells although the receptor loss may not entirely explain the observed desensitization.